Rigi10™ Malleable Penile Prosthesis
Also Known As
Idiopathic hypercalciuria, calcium hyperexcretion, excessive urinary calcium, renal calcium leak, absorptive hypercalciuria, resorptive hypercalciuria, renal phosphate leak hypercalciuria
Definition
Hypercalciuria is a metabolic condition characterized by excessive excretion of calcium in the urine, which significantly increases the risk of calcium-based kidney stone formation.1 It is considered the most common identifiable metabolic risk factor for calcium nephrolithiasis, accounting for approximately 50% of cases.1 The condition can be defined in several ways: traditionally as urinary calcium excretion exceeding 275 mg/day in men and 250 mg/day in women; as excretion greater than 4 mg/kg body weight per day; or as urinary calcium concentration above 200 mg/L.2 Hypercalciuria also contributes to bone demineralization, leading to decreased bone mineral density, osteopenia, and potentially osteoporosis.3 The pathophysiology varies by type, with absorptive hypercalciuria (increased intestinal calcium absorption) being most common, followed by renal leak hypercalciuria (defective renal tubular calcium reabsorption), renal phosphate leak hypercalciuria, and resorptive hypercalciuria (typically from hyperparathyroidism).1
Clinical Context
Hypercalciuria is clinically significant in two primary contexts: as a major risk factor for kidney stone formation and as a contributor to bone demineralization.1 Calcium-based kidney stones (calcium oxalate and calcium phosphate) account for approximately 85% of all kidney stones, with hypercalciuria being the most significant cause of idiopathic calcium-based kidney stones.1 Patient selection for evaluation typically includes those with recurrent kidney stones, unexplained hematuria, or bone density concerns.3 Diagnostic procedures include 24-hour urine collection to measure calcium excretion, serum calcium and parathyroid hormone levels, and sometimes calcium loading tests to determine the specific type of hypercalciuria.2 Treatment approaches vary by type but generally include dietary modifications (moderate calcium intake of 600-800 mg/day, reduced sodium and animal protein, increased fluid intake) and pharmacological interventions such as thiazide diuretics, which enhance renal calcium reabsorption.3 Expected outcomes include reduced stone formation and stabilization of bone mineral density, though long-term management is typically required.1 In pediatric patients, hypercalciuria may present with hematuria, abdominal pain, and urinary symptoms even without stone formation, requiring age-specific diagnostic criteria.1